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Objective-To determine the efficacy of oral nimodipine in reducing cerebral infarction and poor outcomes (death and severe disability) after subarachnoid haemorrhage.Design-Double blind, placebo controlled, randomised trial with three months of follow up and intention to treat analysis. To have an 80% chance with a significance level of 0-05 of detecting a 50% reduction in an incidence of cerebral infarction of 15% a minimum of 540 patients was required.Setting-Four regional neurosurgical units in the United Kingdom.Patients-In all 554 patients were recruited between June 1985 and September 1987 out of a population of 1115 patients admitted with subarachnoid haemorrhage proved by the results of lumbar puncture or computed tomography, or both. The main exclusion criterion was admission to the neurosurgical units more than 96 hours after subarachnoid haemorrhage. There were four breaks of code and no exclusions after entry. One patient was withdrawn and in 130 treatment was discontinued early. All patients were followed up for three months and were included in the analysis, except the patient who had been withdrawn.Interventions-Placebo or nimodipine 60 mg was given orally every four hours for 21 days to 276 and 278 patients, respectively. Treatment was started within 96 hours after subarachnoid haemorrhage.End points -Incidence of cerebral infarction and ischaemic neurological deficits and outcome three months after entry.Measurements-Demographic and clinical data, including age, sex, history of hypertension and subarachnoid haemorrhage, severity ofhaemorrhage according to an adaptation of the Glasgow coma scale, number and site of aneurysms on angiography, and initial findings on computed tomography were measured at entry. Deterioration, defined as development of a focal sign or fall of more than one point on the Glasgow coma scale for more than six hours, was investigated by using clinical criteria and by computed tomography, by lumbar puncture, or at necropsy when appropriate. All episodes of deterioration and all patients with a three month outcome other than a good recovery were assessed by a review committee.Main results-Demographic and clinical data at entry were similar in the two groups. In patients given nimodipine the incidence of cerebral infarction was 22% (61/278) compared with 33% (92/276) in those given placebo, a significant reduction of 34% (95% confidence interval 13 to 50%). Poor outcomes were also significantly reduced by 40% (95% confidence interval 20 to 55%) with nimodipine (20%

SUMMARY Two-hundred and seventeen patients from a total population of 343 patients with arteriovenous malformations, were managed without surgery. Follow up was for a mean of 10-4 years. Using life survival analyses, there was a 42% risk of haemorrhage, 29% risk of death, 18% risk of epilepsy and a 27% risk of having a neurological handicap by 20 years after diagnosis in unoperated patients.

The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.

Sixty-one patients of a population of 343 with cerebral arteriovenous malformations (AVMs) were diagnosed with seizures. Their AVMs were larger (p less than 0.02) and more frequently superficial (p less than 0.05) as compared with the AVMs of patients who were diagnosed with haemorrhage. The factors influencing the development of denovo seizures in patients with diagnosed AVMs were surgical treatment, a presentation with haemorrhage, and age at diagnosis.